Inhibition of Connective Tissue Growth Factor Ameliorates Disease in a Murine Model of Rheumatoid Arthritis

Objective We have shown that connective tissue growth factor (CTGF) plays an important role in the pathogenesis of rheumatoid arthritis (RA). This study was undertaken to evaluate the effects of blockade of the CTGF pathway on the development of collagen‐induced arthritis (CIA) in mice. Methods Arth...

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Published inArthritis & rheumatology (Hoboken, N.J.) Vol. 65; no. 6; pp. 1477 - 1486
Main Authors Nozawa, Kazuhisa, Fujishiro, Maki, Kawasaki, Mikiko, Yamaguchi, Ayako, Ikeda, Keigo, Morimoto, Shinji, Iwabuchi, Kazuhisa, Yanagida, Mitsuaki, Ichinose, Shouzo, Morioka, Megumi, Ogawa, Hideoki, Takamori, Kenji, Takasaki, Yoshinari, Sekigawa, Iwao
Format Journal Article
LanguageEnglish
Published United States Wiley Subscription Services, Inc 01.06.2013
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Abstract Objective We have shown that connective tissue growth factor (CTGF) plays an important role in the pathogenesis of rheumatoid arthritis (RA). This study was undertaken to evaluate the effects of blockade of the CTGF pathway on the development of collagen‐induced arthritis (CIA) in mice. Methods Arthritis was induced in DBA/1J mice by immunization with a combination of type II collagen (CII) and Freund's complete adjuvant. We evaluated the development of arthritis in mice with CIA left untreated versus treated with neutralizing anti‐CTGF monoclonal antibody (mAb). Results Inhibition of CTGF in mice treated with neutralizing anti‐CTGF mAb significantly ameliorated arthritis compared to the untreated mice with CIA. Serum levels of matrix metalloproteinase 3 were reduced by anti‐CTGF mAb treatment. Moreover, blockade of CTGF decreased interleukin‐17 expression on purified CD4+ T lymphocytes. Although the expression of the retinoic acid receptor–related orphan receptor γt gene was not suppressed by anti‐CTGF mAb treatment, that of interferon regulatory factor 4 (IRF‐4) and IκBζ (Nfkbiz), which are other important molecules for the differentiation of Th17 cells, was suppressed. In addition, blockade of CTGF inhibited pathologic proliferation of T lymphocytes in response to CII restimulation in vitro. Moreover, aberrant osteoclastogenesis in mice with CIA was restored by anti‐CTGF mAb treatment. Conclusion Our findings indicate that blockade of CTGF prevents the progression of arthritis in mice with CIA. Anti‐CTGF mAb treatment suppresses pathologic T cell function and restores aberrant osteoclastogenesis in mice with CIA. CTGF may become a new target for the treatment of RA.
AbstractList We have shown that connective tissue growth factor (CTGF) plays an important role in the pathogenesis of rheumatoid arthritis (RA). This study was undertaken to evaluate the effects of blockade of the CTGF pathway on the development of collagen-induced arthritis (CIA) in mice. Arthritis was induced in DBA/1J mice by immunization with a combination of type II collagen (CII) and Freund's complete adjuvant. We evaluated the development of arthritis in mice with CIA left untreated versus treated with neutralizing anti-CTGF monoclonal antibody (mAb). Inhibition of CTGF in mice treated with neutralizing anti-CTGF mAb significantly ameliorated arthritis compared to the untreated mice with CIA. Serum levels of matrix metalloproteinase 3 were reduced by anti-CTGF mAb treatment. Moreover, blockade of CTGF decreased interleukin-17 expression on purified CD4+ T lymphocytes. Although the expression of the retinoic acid receptor-related orphan receptor γt gene was not suppressed by anti-CTGF mAb treatment, that of interferon regulatory factor 4 (IRF-4) and IκBζ (Nfkbiz), which are other important molecules for the differentiation of Th17 cells, was suppressed. In addition, blockade of CTGF inhibited pathologic proliferation of T lymphocytes in response to CII restimulation in vitro. Moreover, aberrant osteoclastogenesis in mice with CIA was restored by anti-CTGF mAb treatment. Our findings indicate that blockade of CTGF prevents the progression of arthritis in mice with CIA. Anti-CTGF mAb treatment suppresses pathologic T cell function and restores aberrant osteoclastogenesis in mice with CIA. CTGF may become a new target for the treatment of RA.
Objective We have shown that connective tissue growth factor (CTGF) plays an important role in the pathogenesis of rheumatoid arthritis (RA). This study was undertaken to evaluate the effects of blockade of the CTGF pathway on the development of collagen-induced arthritis (CIA) in mice. Methods Arthritis was induced in DBA/1J mice by immunization with a combination of type II collagen (CII) and Freund's complete adjuvant. We evaluated the development of arthritis in mice with CIA left untreated versus treated with neutralizing anti-CTGF monoclonal antibody (mAb). Results Inhibition of CTGF in mice treated with neutralizing anti-CTGF mAb significantly ameliorated arthritis compared to the untreated mice with CIA. Serum levels of matrix metalloproteinase 3 were reduced by anti-CTGF mAb treatment. Moreover, blockade of CTGF decreased interleukin-17 expression on purified CD4+ T lymphocytes. Although the expression of the retinoic acid receptor-related orphan receptor [gamma]t gene was not suppressed by anti-CTGF mAb treatment, that of interferon regulatory factor 4 (IRF-4) and I[kappa]B[zeta] (Nfkbiz), which are other important molecules for the differentiation of Th17 cells, was suppressed. In addition, blockade of CTGF inhibited pathologic proliferation of T lymphocytes in response to CII restimulation in vitro. Moreover, aberrant osteoclastogenesis in mice with CIA was restored by anti-CTGF mAb treatment. Conclusion Our findings indicate that blockade of CTGF prevents the progression of arthritis in mice with CIA. Anti-CTGF mAb treatment suppresses pathologic T cell function and restores aberrant osteoclastogenesis in mice with CIA. CTGF may become a new target for the treatment of RA. [PUBLICATION ABSTRACT]
OBJECTIVEWe have shown that connective tissue growth factor (CTGF) plays an important role in the pathogenesis of rheumatoid arthritis (RA). This study was undertaken to evaluate the effects of blockade of the CTGF pathway on the development of collagen-induced arthritis (CIA) in mice.METHODSArthritis was induced in DBA/1J mice by immunization with a combination of type II collagen (CII) and Freund's complete adjuvant. We evaluated the development of arthritis in mice with CIA left untreated versus treated with neutralizing anti-CTGF monoclonal antibody (mAb).RESULTSInhibition of CTGF in mice treated with neutralizing anti-CTGF mAb significantly ameliorated arthritis compared to the untreated mice with CIA. Serum levels of matrix metalloproteinase 3 were reduced by anti-CTGF mAb treatment. Moreover, blockade of CTGF decreased interleukin-17 expression on purified CD4+ T lymphocytes. Although the expression of the retinoic acid receptor-related orphan receptor γt gene was not suppressed by anti-CTGF mAb treatment, that of interferon regulatory factor 4 (IRF-4) and IκBζ (Nfkbiz), which are other important molecules for the differentiation of Th17 cells, was suppressed. In addition, blockade of CTGF inhibited pathologic proliferation of T lymphocytes in response to CII restimulation in vitro. Moreover, aberrant osteoclastogenesis in mice with CIA was restored by anti-CTGF mAb treatment.CONCLUSIONOur findings indicate that blockade of CTGF prevents the progression of arthritis in mice with CIA. Anti-CTGF mAb treatment suppresses pathologic T cell function and restores aberrant osteoclastogenesis in mice with CIA. CTGF may become a new target for the treatment of RA.
Objective We have shown that connective tissue growth factor (CTGF) plays an important role in the pathogenesis of rheumatoid arthritis (RA). This study was undertaken to evaluate the effects of blockade of the CTGF pathway on the development of collagen‐induced arthritis (CIA) in mice. Methods Arthritis was induced in DBA/1J mice by immunization with a combination of type II collagen (CII) and Freund's complete adjuvant. We evaluated the development of arthritis in mice with CIA left untreated versus treated with neutralizing anti‐CTGF monoclonal antibody (mAb). Results Inhibition of CTGF in mice treated with neutralizing anti‐CTGF mAb significantly ameliorated arthritis compared to the untreated mice with CIA. Serum levels of matrix metalloproteinase 3 were reduced by anti‐CTGF mAb treatment. Moreover, blockade of CTGF decreased interleukin‐17 expression on purified CD4+ T lymphocytes. Although the expression of the retinoic acid receptor–related orphan receptor γt gene was not suppressed by anti‐CTGF mAb treatment, that of interferon regulatory factor 4 (IRF‐4) and IκBζ (Nfkbiz), which are other important molecules for the differentiation of Th17 cells, was suppressed. In addition, blockade of CTGF inhibited pathologic proliferation of T lymphocytes in response to CII restimulation in vitro. Moreover, aberrant osteoclastogenesis in mice with CIA was restored by anti‐CTGF mAb treatment. Conclusion Our findings indicate that blockade of CTGF prevents the progression of arthritis in mice with CIA. Anti‐CTGF mAb treatment suppresses pathologic T cell function and restores aberrant osteoclastogenesis in mice with CIA. CTGF may become a new target for the treatment of RA.
Author Ikeda, Keigo
Sekigawa, Iwao
Ichinose, Shouzo
Takamori, Kenji
Ogawa, Hideoki
Yamaguchi, Ayako
Morioka, Megumi
Yanagida, Mitsuaki
Kawasaki, Mikiko
Morimoto, Shinji
Takasaki, Yoshinari
Iwabuchi, Kazuhisa
Fujishiro, Maki
Nozawa, Kazuhisa
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Snippet Objective We have shown that connective tissue growth factor (CTGF) plays an important role in the pathogenesis of rheumatoid arthritis (RA). This study was...
We have shown that connective tissue growth factor (CTGF) plays an important role in the pathogenesis of rheumatoid arthritis (RA). This study was undertaken...
Objective We have shown that connective tissue growth factor (CTGF) plays an important role in the pathogenesis of rheumatoid arthritis (RA). This study was...
OBJECTIVEWe have shown that connective tissue growth factor (CTGF) plays an important role in the pathogenesis of rheumatoid arthritis (RA). This study was...
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SubjectTerms Animals
Antibodies, Monoclonal - immunology
Antibodies, Monoclonal - pharmacology
Arthritis, Experimental - drug therapy
Arthritis, Experimental - immunology
Arthritis, Rheumatoid - drug therapy
Arthritis, Rheumatoid - immunology
Connective Tissue Growth Factor - antagonists & inhibitors
Disease Models, Animal
Enzyme-Linked Immunosorbent Assay
Immunoblotting
Immunohistochemistry
Lymphocyte Activation - drug effects
Lymphocyte Activation - immunology
Medical research
Mice
Mice, Inbred DBA
Microarray Analysis
Real-Time Polymerase Chain Reaction
Title Inhibition of Connective Tissue Growth Factor Ameliorates Disease in a Murine Model of Rheumatoid Arthritis
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fart.37902
https://www.ncbi.nlm.nih.gov/pubmed/23436223
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https://search.proquest.com/docview/1364707252
Volume 65
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